The symptoms of schizophrenia, obsessive-compulsive disorder (OCD), and Tourette's syndrome result in part from sensorimotor gating deficits. Patients diagnosed with these disorders have deficient prepulse inhibition (PPI) (a measure of sensorimotor gating). Additionally, schizophrenia patients have startle habitation deficits. The serotonin system has been implicated in both the pathophysiology and the mechanism of action of therapeutics for these disorders. A better understanding of the neural mechanisms that modulate PPI and habitation (two forms of startle plasticity) could permit the development of better treatments. This project proposes to investigate the role of pre- and postsynaptic serotonin-1B (5-HT1B) receptors and specific neural circuits in modulating PPI and habituation. 5-HT1B receptors regulate the activity of dopamine, serotonin, and GABA neurons that have been shown to modulate PPI.